This invention is directed to a method and an apparatus for artificially ventilating patients--especially young infants--and in particular, to a ventilation method which utilizes electronically predetermined pressure control for the minimization of work done on lung tissues.
The ideas proposed grew out of observation that newborn infants who require prolonged mechanical ventilation are subject to a variety of complications that increase in frequency with time on the respirator. Such conditions as pneumothorax (rupture of the lung), mediastinal emphysema (air in the mid-chest), circulatory compromise [J. H. Comroe, Physiology of Respiration, Year Book Med. Publ. Inc., Chicago, 1970, Sec. Ed.], bronchopulmonary dysplasia [W. H. Northway et al, Pulmonary disease following respirator therapy of hyaline membrane disease--bronchopulmonary dysplasia, N. Eng. J. Med. 276, 357, 1967], and oxygen toxicity [D. K. Edwards et al, Twelve years' experience with broncho pulmonary dysplasia, Ped. Vol. 59, 839-846, 1977], have all been related to the use of current mechanical ventilators.
Much research has gone into isolating the factors responsible for lung damage. Though there is controversy in this area, it seems to be generally accepted that high oxygen concentrations [B. E. Welch et al, Time concentration effects in relation to oxygen toxicity in man, Federation Proc. 22, 1053-1056, 1963] and high peak airway pressures [A. Taghizadeh et al, Pathogenesis of bronchopulmonary dysplasia following hyaline membrane disease, Am. J. Path. 82, 241-264, 1976] are linked to pathological outcomes. The difficulty in mitigating these factors has been the requirement to provide patients with adequate ventilation in the face of stiff compromised lungs.
The dilemma is particularly acute in the case of newborn infants with Respiratory Distress Syndrome (a condition of lung immaturity and deficiency of surfactant material) where prolonged respirator therapy may be required. The most dreaded long term complication, bronchopulmonary dysplasia (destructive fibroplastic changes in lung tissue), can result in fatality or chronic pulmonary insufficiency lasting months or years. Though the precise cause of this condition is not clear, a retrospective pathological study done by A. Taghizadeh (mentioned above) has implicated the use of high peak airway pressures. It is of interest that in clinical trials with infants [E. O. R. Reynolds et al, Improved prognosis of infants mechanically ventilated for hyaline membrane disease, Arch. Dis. Child. 49, 505, 1974], the lowering of peak airway pressures; slowing of respiratory frequencies and increasing of inspiratory to expiratory time ratios has resulted in improved survival largely by reducing the overall incidence of bronchopulmonary dysplasia. Other work [J. Stocks et al, The tole of artificial ventilation, oxygen and CPAP in the pathogenesis of lung damage in neonates: Assessment by serial measurements of lung function, Ped. Vo. 57, 352-362, 1976; and J. Stocks et al, Airway resistance in infants after various treatments for hyaline membrane disease: Special emphasis on prolonged high levels of inspired oxygen, Ped. 61, 178-183, 1978] has also implicated high pressure as a factor while the contribution of high oxygen concentration alone has been questioned [A. G. S. Philip, Oxygen plus pressure plus time: The etiology of broncho pulmonary dysplasia, Ped. Vol. 55, no. 1, Jan. 1975; and V. A. Pusey et al, Pulmonary fibroplasia following prolonged artificial ventilation of newborn infants, Can. Med. Assoc. 100, 451, 1969].
Though current research in this area has been focussing on the effects of various pressure wave forms on respiration [S. J. Boros, Variations in inspiratory:expiratory ratio and airway pressure wave form during mechanical ventilation: The significance of mean airway pressure, J. of Ped., Vol. 94, no. 1, 114-117, 1979], mechanical ventilators now in use are limited in providing either sinusoidal, square or triangular waves which must be manually set with regard to amplitude, frequency and duration. Though adequate blood gas values are the criteria used by the medical operator, there is currently no good way in which he can adjust for changing lung parameters such as resistance and compliance. Thus there is little control of the pressure damage or work done on the tissues being inflated.
A mathematical analysis of the data of Reynolds et al (mentioned above) comparing their modified wave form (low frequency, long inspiratory cycle, square wave) with others commonly in use (high frequency, short inspiration cycle, square or sinusoidal wave) suggests that the calculated quantity of work done is significantly less in the former despite comparable peak pressures.
Most respirator or ventilator systems which are presently used have been designed to deliver a preselected volume of gas to a patient. These are exemplified by U.S. Pat. No. 3,834,381, issued Sept. 19, 1974 to V. M. Peterson; U.S. Pat. No. 3,905,362, issued Sept. 16, 1975 to T. B. Eyrick et al; U.S. Pat. No. 3,985,131, issued Oct. 12, 1976 to K. E. Buck et al; and U.S. Pat. No. 4,036,221, issued July 19, 1977 to D. Hillsman et al. These devices though mainly concerned with the volume of gas delivered per inspiration/expiration cycle may also place limitations on other parameters in the gas delivery system. U.S. Pat. No. 3,905,362 places a preselected limit on the flow rate. U.S. Pat. No. 3,985,131 has a pair of different size volume chambers to provide a choice of ventilating modes. U.S. Pat. No. 4,036,221 includes a feedback circuit for assuring that the desired volume waveform is followed during each cycle.
Other respirators are pressure controlled, and usually interrupt gas flow when a predetermined pressure is reached at the patient. U.S. Pat. No. 3,961,627 monitors gas flow and pressure at the patient, these measurements are compared to values fixed by the doctor for adjustment of the control valve.